I have argued that the original function of ubiquitously expressed beta 2-microglobulin-MHC antigen dimers has always been to serve as the plasma membrane anchorage sites of organogenesis-directing antigens, such as testis-organizing H-Y, and it is for this reason that all parasitic viruses evolved the strategy of displacing those functionally critical host antigens with their own; hence, observed H-2 restrictions in the mouse of T-cell killings of H-Y incompatible as well as virally infected or transformed targets. Extensive allelic polymorphisms of the MHC gene complex, seen in all mammalian species, as well as increasing instances of disease associations with HLA haplotypes, seen in man, can readily be understood if one realizes that numerous allelic forms of MHC antigens are likely to offer different binding affinities to multitudes of organogenesis-directing as well as viral antigens. In this manner, allelic polymorphisms of the MHC loci greatly influence the life expectancy of individuals. Using the Beta 2-m (-), HLA (-) human male Daudi cell line and Daudi X Hela (males x females) somatic hybrids, we shall obtain conclusive evidence of the physical association between H-Y and Beta 2-m-HLA antigen dimers. Using congenic mouse strains, one of which expresses viral gp70 antigen, we shall also test the competitive displacement of H-Y by gp70.